ArticleIranian journal of pharmaceutical research : IJPR
Quercetin Inhibits Gastric Cancer Progression via Suppression of HOTAIR/mir-217/GPC5 Axis.
Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Long noncoding RNA (lncRNA) hox transcript antisense intergenic RNA (HOTAIR) is implicated in the progression of gastric cancer (GC) by promoting the microRNA-217 (miR-217)-glypican-5 (GPC5) axis. Quercetin (QCT), a well-known flavonoid, has demonstrated anticancer effects against various malignancies, including GC. However, the impact of QCT on HOTAIR expression and its downstream mediators remains unclear. Objectives: This study aimed to elucidate the antitumor mechanisms of QCT and its regulatory effects on the HOTAIR/miR-217/GPC5 axis in AGS and MKN-45 GC cell lines. Methods: Cellular viability, apoptosis, cell cycle progression, invasion, and oxidative stress markers were assessed using the MTT assay, annexin V-FITC/PI staining, real-time quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and spectrophotometry. Expression levels of HOTAIR, miR-217, and GPC5 were quantified. Results: The QCT significantly downregulated HOTAIR and GPC5 while upregulating miR-217 in both cell lines (P < 0.001). The QCT induced dose-dependent apoptosis and cell cycle arrest, and reduced invasion through upregulation of TP53/PTEN (P < 0.05). Oxidative stress modulation displayed lineage-specific differences, with a marked reduction in malondialdehyde (MDA) in MKN-45 cells (P = 0.013). AGS cells exhibited greater sensitivity to QCT than MKN-45 cells. Conclusions: These findings highlight QCT's ability to inhibit GC progression via the HOTAIR/miR-217/GPC5 axis, with molecular heterogeneity influencing therapeutic response. The QCT emerges as a promising candidate for further investigation as a multifaceted agent against GC, though validation in preclinical models is necessary.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.